Professor Colin Raston of Flinders University in Adelaide created the
vortex fluidic device after he did some brainstorming during a long
haul flight between Los Angeles and Sydney.
"The design was actually put together on that 15-hour flight and the rest is history," he said.
"We now have these devices that are delivering stunning results."
The
vortex fluidic device was first tested recently on a hen egg, and
researchers managed to pull apart its tangled proteins and return the
egg white to an earlier state.
Professor Raston said the device
allowed more tightly controlled chemical processes to be performed,
saving researchers time and reducing their materials wastage. One
application already found allows improved delivery of a common cancer
treatment drug, Carboplatin, which is used against ovarian and lung
cancers. The device has allowed drug potency to be boosted as much as four-and-a-half-times, Professor Raston said.
"The drug is released at the tumor so the consequence of that, is you need less drug and you reduce the side-effects."In
terms of the bigger picture, you're minimising the amount of drug that
ends up as waste because most of the drugs we take end up in the waste,
in sewage."
"It gives us the promise of offering an alternative where we have
more drug being delivered to the tumor and less drug being delivered to
the rest of the body," he said.
"That means less side-effects for the patient and hopefully a much better effect in terms of tumor response."What this group is doing is an example of one drug but we would hope we could extend this to many drugs."
Friday, May 22, 2015
Clinical Trial of diabetes drug for Ovarian Cancer
The University of Chicago Medicine is leading, with two other
centers, a clinical trial that will compare the most effective current
therapy for patients with stage 3 or stage 4 Ovarian Cancer against that
same therapy plus Metformin. To enroll in the trial, volunteers must
have a presumed or confirmed diagnosis of ovarian, fallopian tube, or
primary peritoneal carcinoma, but not diabetes.
"This is the first study of its kind in ovarian cancer," said trial director Diane Yamada, MD, professor of obstetrics and gynecology at the University of Chicago. "We think this is an exciting opportunity to find out if a safe, well-tested and inexpensive drug can significantly improve on our best current therapy. There is a strong biological rationale, a series of consistently encouraging results from observational studies, and a real need for better, cost-effective therapies for this type of cancer."
Studies performed at the University of Chicago and at the Mayo Clinic have independently found that ovarian cancer patients who happened to be taking metformin for their diabetes while going through cancer treatment had significantly better outcomes. In the Chicago study, 63 percent of patients taking metformin for their diabetes were alive five years later, compared with 37 percent of patients who did not have diabetes and 23 percent of patients who had diabetes but were not taking metformin.
"This is the first study of its kind in ovarian cancer," said trial director Diane Yamada, MD, professor of obstetrics and gynecology at the University of Chicago. "We think this is an exciting opportunity to find out if a safe, well-tested and inexpensive drug can significantly improve on our best current therapy. There is a strong biological rationale, a series of consistently encouraging results from observational studies, and a real need for better, cost-effective therapies for this type of cancer."
Studies performed at the University of Chicago and at the Mayo Clinic have independently found that ovarian cancer patients who happened to be taking metformin for their diabetes while going through cancer treatment had significantly better outcomes. In the Chicago study, 63 percent of patients taking metformin for their diabetes were alive five years later, compared with 37 percent of patients who did not have diabetes and 23 percent of patients who had diabetes but were not taking metformin.
UK study of Prostate Cancer gene map for targeted drugs
Scientists have unveiled a comprehensive genetic map of advanced Prostate Cancer, hailing it as the disease's "Rosetta Stone".
The study was led in the UK by scientists at the Institute of Cancer Research (ICR) London in collaboration with several teams in the United States.
Researchers analyzed the genetic codes of tumors from 150 patients with metastatic - or advanced - prostate cancer, whose disease had spread to other parts of the body.
They found that 89% had genetic aberrations for which there were existing drugs or treatments undergoing clinical trials.
Prof Johann de Bono, of the ICR and Royal Marsden NHS Foundation Trust told the BBC: "This is truly a game-changer. We are calling this prostate cancer's Rosetta Stone, because we can now decode the disease for the first time.
"In the past, we used to treat lethal prostate cancer as a single illness but this shows that it is a group of diseases, each driven by their own set of mutations."
Prof de Bono said it meant that, using genetic testing, it would be possible to individualize patient care, heralding the arrival of personalized treatment for advanced prostate cancer.
More than 40,000 men are diagnosed with prostate cancer and nearly 11,000 die in the UK each year.
The study was led in the UK by scientists at the Institute of Cancer Research (ICR) London in collaboration with several teams in the United States.
Researchers analyzed the genetic codes of tumors from 150 patients with metastatic - or advanced - prostate cancer, whose disease had spread to other parts of the body.
They found that 89% had genetic aberrations for which there were existing drugs or treatments undergoing clinical trials.
Prof Johann de Bono, of the ICR and Royal Marsden NHS Foundation Trust told the BBC: "This is truly a game-changer. We are calling this prostate cancer's Rosetta Stone, because we can now decode the disease for the first time.
"In the past, we used to treat lethal prostate cancer as a single illness but this shows that it is a group of diseases, each driven by their own set of mutations."
Prof de Bono said it meant that, using genetic testing, it would be possible to individualize patient care, heralding the arrival of personalized treatment for advanced prostate cancer.
More than 40,000 men are diagnosed with prostate cancer and nearly 11,000 die in the UK each year.
Radiations' evolving choices in Cancer Treatment
"Most radiation is done with 'external radiation,' which is delivered
from outside the body, with X-rays or electrons with a machine called a
linear accelerator," says Dr. Matthew Katz, medical director of
radiation oncology at Lowell General Hospital in Massachusetts.
The technology keeps improving, Katz say, from the early 1990s when CT scans first allowed oncologists to treat tumors in 3-D to current techniques. One is intensity modulated radiation therapy or IMRT, which shapes the beams more precisely and sends stronger radiation doses to some parts of the body and weaker doses to others. Continued improvements allow practitioners "to more accurately target common cancers better than before," he says. "That accuracy ensures we're more comfortable that the cancer is receiving treatment rather than the normal tissue, and in many cases can also lessen side effects." Then there are the high-dose, ultraprecise types of radiation (including the brands Gamma Knife and CyberKnife). "Stereotactic radiation was used originally for brain metastasis, cancer spread to the brain, where the accuracy needed to be within a millimeter," Katz says. Now, he continues, it's improving cure rates for inoperable early-stage lung cancer, and other uses are increasing. "All need more research," he adds.
Proton beam therapy is coming to the University of Maryland Medical Center within the year, Tyer says. It uses protons instead of X-rays and is meant to deliver more radiation to tumors while decreasing radiation to healthy tissue.
Because the cyclotron machine costs tens of millions of dollars and requires specialized staff, only a handful of U.S. centers offer it, and availability is limited.
Dr. Bruce Haffty, chair of the board of directors for American Society for Radiation Oncology, or ASTRO, says while proton radiation has been around for decades, it was largely experimental. Now, with nearly 20 facilities nationwide, he expects every state to have one within a few years. More types of patients will benefit as availability increases, he says, and as data from clinical trials unfold.
The technology keeps improving, Katz say, from the early 1990s when CT scans first allowed oncologists to treat tumors in 3-D to current techniques. One is intensity modulated radiation therapy or IMRT, which shapes the beams more precisely and sends stronger radiation doses to some parts of the body and weaker doses to others. Continued improvements allow practitioners "to more accurately target common cancers better than before," he says. "That accuracy ensures we're more comfortable that the cancer is receiving treatment rather than the normal tissue, and in many cases can also lessen side effects." Then there are the high-dose, ultraprecise types of radiation (including the brands Gamma Knife and CyberKnife). "Stereotactic radiation was used originally for brain metastasis, cancer spread to the brain, where the accuracy needed to be within a millimeter," Katz says. Now, he continues, it's improving cure rates for inoperable early-stage lung cancer, and other uses are increasing. "All need more research," he adds.
Proton beam therapy is coming to the University of Maryland Medical Center within the year, Tyer says. It uses protons instead of X-rays and is meant to deliver more radiation to tumors while decreasing radiation to healthy tissue.
Because the cyclotron machine costs tens of millions of dollars and requires specialized staff, only a handful of U.S. centers offer it, and availability is limited.
Dr. Bruce Haffty, chair of the board of directors for American Society for Radiation Oncology, or ASTRO, says while proton radiation has been around for decades, it was largely experimental. Now, with nearly 20 facilities nationwide, he expects every state to have one within a few years. More types of patients will benefit as availability increases, he says, and as data from clinical trials unfold.
Thursday, May 21, 2015
New technology boosts potency of Targeted Cancer Therapy
In work that heralds a new, more potent form of targeted therapy for
cancer, Dana-Farber Cancer Institute scientists have devised a chemical
technology that doesn't just disable malevolent proteins in tumor cells,
as current agents do, but destroys them. The strategy uses tumor cells' own protein-chopping machinery to break down and dispose of proteins that drive cancer growth.
When tested in laboratory samples of leukemia cells and in animals with
human-like leukemia, the approach caused cancer cells to die much more
quickly than with conventional targeted therapies.
Researchers developed the strategy as a way to develop inhibitors of "undruggable" proteins and overcome drug resistance, a common shortcoming of targeted therapies. Resistance arises when tumors that originally responded to a particular therapy manage to circumvent the drug's effects and resume their growth. "One of the reasons resistance occurs is that cancer-related proteins often have multiple functions within the cell, and conventional targeted therapies inhibit just one or a few of those functions," said the paper's senior author, James Bradner, MD, an oncologist and chemist at Dana-Farber. "Conventional drugs allow the targeted protein to adapt to the drug, and the cell finds alternate routes for its growth signals. "We began designing approaches that cause the target protein to disintegrate, rather than merely be inhibited," he continued. "It would be very powerful if we could chemically convert an inhibitor drug into a degrader drug."The team tested the technology - which they dubbed "degronimids",in laboratory samples of leukemia cells. They began with the drug JQ1, which inhibits BRD4, a protein that orchestrates the expression of cancer growth genes. They built an adapter out of phthalimide - a chemical derivative of the drug thalidomide - and attached it to JQ1. The phthalimide was designed to bind snugly to a protein-degrading enzyme E3 (called Cereblon), making it ideal as a trailer hitch. When investigators treated the leukemia cells with a JQ1-and-phthalimide "conjugate" called dBET1, the BRD4 protein within the cells was degraded in less than an hour."We're very excited that this chemical technology may offer a way to improve many cancer drug molecules, and of course this strategy has implications beyond cancer for the treatment of other life-threatening diseases," Bradner said.
Researchers developed the strategy as a way to develop inhibitors of "undruggable" proteins and overcome drug resistance, a common shortcoming of targeted therapies. Resistance arises when tumors that originally responded to a particular therapy manage to circumvent the drug's effects and resume their growth. "One of the reasons resistance occurs is that cancer-related proteins often have multiple functions within the cell, and conventional targeted therapies inhibit just one or a few of those functions," said the paper's senior author, James Bradner, MD, an oncologist and chemist at Dana-Farber. "Conventional drugs allow the targeted protein to adapt to the drug, and the cell finds alternate routes for its growth signals. "We began designing approaches that cause the target protein to disintegrate, rather than merely be inhibited," he continued. "It would be very powerful if we could chemically convert an inhibitor drug into a degrader drug."The team tested the technology - which they dubbed "degronimids",in laboratory samples of leukemia cells. They began with the drug JQ1, which inhibits BRD4, a protein that orchestrates the expression of cancer growth genes. They built an adapter out of phthalimide - a chemical derivative of the drug thalidomide - and attached it to JQ1. The phthalimide was designed to bind snugly to a protein-degrading enzyme E3 (called Cereblon), making it ideal as a trailer hitch. When investigators treated the leukemia cells with a JQ1-and-phthalimide "conjugate" called dBET1, the BRD4 protein within the cells was degraded in less than an hour."We're very excited that this chemical technology may offer a way to improve many cancer drug molecules, and of course this strategy has implications beyond cancer for the treatment of other life-threatening diseases," Bradner said.
UK researchers usher in New Era for Prostate Cancer Trials
The vast majority of advanced prostate tumors contain genetic faults that make them sensitive to drugs already available or in development, according to a major study. Previous large-scale genetic studies of prostate cancer have tended to
rely on tumor samples taken from men at earlier stages of the disease. The new study, a collaboration between researchers at eight centres
across the US and the UK, took biopsy samples from 150 men who had
previously had surgery to remove their prostate tumour, and hormone
treatment, after which their disease had spread and become resistant. The tumor samples were taken from the men’s lymph nodes, bone, liver and other tissues.
Around 90 per cent of them were found to contain previously-known DNA errors, linked to sensitivity to existing or experimental drugs.
About a quarter of the samples contained faults in genes like BRCA1, BRCA2 and ATM, which are involved in DNA repair. Faults in these genes are linked to sensitivity to drugs called PARP inhibitors, originally developed to treat breast and ovarian cancers but now being tested in prostate cancer.
“This study provides a strong argument that the genomics driving advanced prostate cancer is fundamentally different than primary prostate cancer”, said Dr Eliezer Van Allen, from Dana-Farber Cancer Institute, one of the study’s lead authors.
Professor Johann de Bono, from The Institute of Cancer Research in London, where some of the work was carried out, said the findings were “hugely encouraging”.
Around 90 per cent of them were found to contain previously-known DNA errors, linked to sensitivity to existing or experimental drugs.
About a quarter of the samples contained faults in genes like BRCA1, BRCA2 and ATM, which are involved in DNA repair. Faults in these genes are linked to sensitivity to drugs called PARP inhibitors, originally developed to treat breast and ovarian cancers but now being tested in prostate cancer.
“This study provides a strong argument that the genomics driving advanced prostate cancer is fundamentally different than primary prostate cancer”, said Dr Eliezer Van Allen, from Dana-Farber Cancer Institute, one of the study’s lead authors.
Professor Johann de Bono, from The Institute of Cancer Research in London, where some of the work was carried out, said the findings were “hugely encouraging”.
Tuesday, May 19, 2015
New Cancer Treatment studies show major advances
The American Society of Clinical Oncology (ASCO) announced results
from four major studies to be presented at ASCO's 51st Annual Meeting,
May 29-June 2, in Chicago. Findings showed that use of a widely
available Vitamin pill reduces the risk of non-melanoma Skin Cancers;
that early chemotherapy extends the lives of men with advanced Prostate Cancers; and that new therapies can improve outcomes for children with a
rare form of Kidney Cancer and adults with relapsed multiple myeloma.
"Trials like these are engines of progress for people with cancer of all ages," said ASCO President Peter Paul Yu, MD, FACP, FASCO. "In just four studies, we see the potential to spare thousands of people the stress and complications of a new cancer diagnosis, and to extend the lives of children and adults facing cancer in its most daunting forms. At ASCO's meeting in Chicago, we'll continue to see the transformative power of investments in cancer research and care."
"We're in an era of cutting-edge precision medicine, yet we can still achieve meaningful progress with conventional treatments," said Gregory A. Masters, MD, FACP, FASCO, Chair of ASCO's Cancer Communications Committee. "Thanks to a deeper understanding of cancer biology, we have a potential new targeted therapy for multiple myeloma, and can better tailor treatment for kids with Wilms tumor. At the same time, a simple vitamin pill and a long-available chemotherapy are being put to work in different ways to improve the lives of patients."
"Trials like these are engines of progress for people with cancer of all ages," said ASCO President Peter Paul Yu, MD, FACP, FASCO. "In just four studies, we see the potential to spare thousands of people the stress and complications of a new cancer diagnosis, and to extend the lives of children and adults facing cancer in its most daunting forms. At ASCO's meeting in Chicago, we'll continue to see the transformative power of investments in cancer research and care."
"We're in an era of cutting-edge precision medicine, yet we can still achieve meaningful progress with conventional treatments," said Gregory A. Masters, MD, FACP, FASCO, Chair of ASCO's Cancer Communications Committee. "Thanks to a deeper understanding of cancer biology, we have a potential new targeted therapy for multiple myeloma, and can better tailor treatment for kids with Wilms tumor. At the same time, a simple vitamin pill and a long-available chemotherapy are being put to work in different ways to improve the lives of patients."
A new frontier in Cancer Treatment, kinder and gentler
Researchers at Oregon State University are pursuing a new concept in
treatment of epithelial cancer, especially head and neck cancer, by
using two promising "analogs" of an old compound that was once studied
as a potent anti-tumor agent, but long ago abandoned because it was too
toxic.
The analogs are more highly selective than the parent compound, Pactamycin, which originally was found to kill all cells, from bacteria to mammals, by inhibiting their protein synthesis.
The pactamycin analogs, which were developed with biosynthetic engineering, also offer a different approach toward cancer therapy, an effort to essentially put cancer cells to sleep, instead of killing them. If successful, this trend may herald a new future in "kinder and gentler" cancer treatments.
The effects of the pactamycin analogs, called TM-025 and TM-026, were characterized in head and neck cancer cell lines, which cause the eighth most common cancer in the world. But they may have applications to a wider range of cancers, the researchers said, particularly melanoma.
"A traditional view of chemotherapy is that you try to completely kill cancer cells and destroy tumors," said Arup Indra, an associate professor in the OSU College of Pharmacy and one of the lead authors on the study. "Sometimes this is effective, sometimes not as much. An alternative approach is to cause rapid cell aging and induce premature senescence, which we believe could become
The effects of the pactamycin analogs, called TM-025 and TM-026, were characterized in head and neck cancer cell lines, which cause the eighth most common cancer in the world. But they may have applications to a wider range of cancers, the researchers said, particularly melanoma.
"A traditional view of chemotherapy is that you try to completely kill cancer cells and destroy tumors," said Arup Indra, an associate professor in the OSU College of Pharmacy and one of the lead authors on the study. "Sometimes this is effective, sometimes not as much. An alternative approach is to cause rapid cell aging and induce premature senescence, which we believe could become a new frontier in cancer drug development."
The analogs are more highly selective than the parent compound, Pactamycin, which originally was found to kill all cells, from bacteria to mammals, by inhibiting their protein synthesis.
The pactamycin analogs, which were developed with biosynthetic engineering, also offer a different approach toward cancer therapy, an effort to essentially put cancer cells to sleep, instead of killing them. If successful, this trend may herald a new future in "kinder and gentler" cancer treatments.
The effects of the pactamycin analogs, called TM-025 and TM-026, were characterized in head and neck cancer cell lines, which cause the eighth most common cancer in the world. But they may have applications to a wider range of cancers, the researchers said, particularly melanoma.
"A traditional view of chemotherapy is that you try to completely kill cancer cells and destroy tumors," said Arup Indra, an associate professor in the OSU College of Pharmacy and one of the lead authors on the study. "Sometimes this is effective, sometimes not as much. An alternative approach is to cause rapid cell aging and induce premature senescence, which we believe could become
The effects of the pactamycin analogs, called TM-025 and TM-026, were characterized in head and neck cancer cell lines, which cause the eighth most common cancer in the world. But they may have applications to a wider range of cancers, the researchers said, particularly melanoma.
"A traditional view of chemotherapy is that you try to completely kill cancer cells and destroy tumors," said Arup Indra, an associate professor in the OSU College of Pharmacy and one of the lead authors on the study. "Sometimes this is effective, sometimes not as much. An alternative approach is to cause rapid cell aging and induce premature senescence, which we believe could become a new frontier in cancer drug development."
Monday, May 18, 2015
New release of Glioblastoma Cancer Atlas helps researchers
Robust new data added to the Ivy Glioblastoma Atlas Project (Ivy GAP)
changes the scope and impact of this publicly available resource for
researchers and clinicians searching for treatments for this most deadly
and aggressive of brain cancers, glioblastoma multiforme. Led by researchers at the Allen Institute for Brain Science and
Swedish Neuroscience Institute and funded with a grant from The Ben and
Catherine Ivy Foundation, Ivy GAP includes detailed information about
genes expressed in the various anatomical regions of glioblastoma and
important data about the presumed initial cancer stem cells that lead to
tumor formation.
"This atlas has been a long-term partnership to provide a public resource for researchers worldwide to mine the data and identify trends that may lead to further studies and treatments," says Allan Jones, Ph.D., CEO of the Allen Institute."Our ultimate goal is to change the outcome for patients with this devastating disease," says Ralph Puchalski, Ph.D., scientist at the Allen Institute for Brain Science and co-Principal Investigator on the project. "The Ivy Glioblastoma Atlas Project is an unprecedented platform for exploring the anatomic and genetic basis of glioblastoma at the cellular and molecular levels. The atlas is an anatomic tour de force that is sure to provide vital information into how such tumors grow and invade healthy brain tissue."
"The need for projects like the Ivy Glioblastoma Atlas Project is urgent," said Catherine Ivy, president of The Ben and Catherine Ivy Foundation. "If we can give our medical leaders better research tools, we can move closer to our ultimate goal of curing glioblastoma."
"This atlas has been a long-term partnership to provide a public resource for researchers worldwide to mine the data and identify trends that may lead to further studies and treatments," says Allan Jones, Ph.D., CEO of the Allen Institute."Our ultimate goal is to change the outcome for patients with this devastating disease," says Ralph Puchalski, Ph.D., scientist at the Allen Institute for Brain Science and co-Principal Investigator on the project. "The Ivy Glioblastoma Atlas Project is an unprecedented platform for exploring the anatomic and genetic basis of glioblastoma at the cellular and molecular levels. The atlas is an anatomic tour de force that is sure to provide vital information into how such tumors grow and invade healthy brain tissue."
"The need for projects like the Ivy Glioblastoma Atlas Project is urgent," said Catherine Ivy, president of The Ben and Catherine Ivy Foundation. "If we can give our medical leaders better research tools, we can move closer to our ultimate goal of curing glioblastoma."
Newly designed investigational Cancer Stem Cell pathway Inhibitors
Boston Biomedical,
an industry leader in the development of novel compounds designed to
target cancer stem cell (CSC) pathways, will present clinical data on
the investigational compounds BBI608 and BBI503 in multiple tumor types
at the 2015 American Society of Clinical Oncology annual meeting, held
from May 29 to June 2, 2015, in Chicago, IL.
Data
to be highlighted at the meeting show the potential of BBI608, an
orally-administered investigational agent that targets STAT3, leading to
inhibition of the critical genes for maintaining cancer stemness for
anti-cancer activity when used in combination with other
chemotherapeutics across varying advanced cancers, including Gastric and Colorectal. The study protocol from the BRIGHTER study, the phase 3
clinical trial currently underway to investigate cancer stem cell
pathway inhibitors, will also be showcased.
Additional
data featuring BBI503,an orally-administered investigational agent
designed to inhibit Nanog and other cancer stem cell pathways by
targeting kinases showed encouraging early signs of anti-cancer activity
for patients with advanced Colorectal Cancer.
Friday, May 15, 2015
Contraceptive and cholesterol-lowering drugs used to treat Cancer
The combination of a cholesterol-lowering drug, Bezafibrate, and a
contraceptive steroid, Medroxyprogesterone Acetate, could be an
effective, non-toxic treatment for a range of cancers, researchers at
the University of Birmingham have found.
Early stage clinical trials of the drugs in elderly patients with acute myeloid leukaemia (AML) have shown promising results, with survival three months longer on average than standard palliative care. The combination, known as BaP, has also been used alongside chemotherapy to successfully treat children with Burkitt's lymphoma (BL), the most common childhood cancer in Eastern Africa.
Until now it was uncertain whether the activity of the drugs against these two very different blood cancers was mediated by a common mechanism or by different effects in each cancer type.
The scientists, who were funded by Leukaemia & Lymphoma Research, used state of the art technology to interrogate the drug's effects on the metabolism and chemical make-up of AML and BL cells and found that in both cell types the drugs block an enzyme crucial to the production of fatty acids, which cancer cells need to grow and multiply. They also demonstrated that the ability of BaP treatment to deactivate this enzyme, called stearoyl CoA desaturase, was what prompted cancer cells to die.
Early stage clinical trials of the drugs in elderly patients with acute myeloid leukaemia (AML) have shown promising results, with survival three months longer on average than standard palliative care. The combination, known as BaP, has also been used alongside chemotherapy to successfully treat children with Burkitt's lymphoma (BL), the most common childhood cancer in Eastern Africa.
Until now it was uncertain whether the activity of the drugs against these two very different blood cancers was mediated by a common mechanism or by different effects in each cancer type.
The scientists, who were funded by Leukaemia & Lymphoma Research, used state of the art technology to interrogate the drug's effects on the metabolism and chemical make-up of AML and BL cells and found that in both cell types the drugs block an enzyme crucial to the production of fatty acids, which cancer cells need to grow and multiply. They also demonstrated that the ability of BaP treatment to deactivate this enzyme, called stearoyl CoA desaturase, was what prompted cancer cells to die.
High-tech Cancer Treatment comes to North Texas
Inside a new three-story facility in Irving,Texas, a team of physicists,
engineers and medical doctors is working on a new tool to fight cancer,
all directed by one of the leading radiation oncologists in the country. "I
found the Proton Therapy to be not only very effective, but our
published reports on the toxicity profile, and patient satisfaction
rates have been quite good," medical director Dr. Andrew Lee explained.
During treatment a highly concentrated proton beam is shot into a cancerous tumor. The beam is generated by something called a particle accelerator, which speeds up the particles to roughly 60 percent of the speed of light. They head down a specially designed pathway, to be diverted to one of three treatment rooms. Once the protons reach the treatment room, they are concentrated into a beam that is aimed right at the cancerous cells. To make it as accurate as possible, a giant, three-story machine rotates the beam around the patient. SMU Physics Professor Steve Sekula says proton therapy is a great example of theoretical work yielding a practical result.
During treatment a highly concentrated proton beam is shot into a cancerous tumor. The beam is generated by something called a particle accelerator, which speeds up the particles to roughly 60 percent of the speed of light. They head down a specially designed pathway, to be diverted to one of three treatment rooms. Once the protons reach the treatment room, they are concentrated into a beam that is aimed right at the cancerous cells. To make it as accurate as possible, a giant, three-story machine rotates the beam around the patient. SMU Physics Professor Steve Sekula says proton therapy is a great example of theoretical work yielding a practical result.
British trial shows Prostate Cancer drug extends lives
Docetaxel is normally given after hormone treatment has failed. But
results, to be presented at the American Society of Clinical Oncology,
will show earlier treatment can extend life expectancy from 43 to 65
months.
Experts said the findings from a trial in Britain and Switzerland were "potentially game-changing".
More than 40,000 men are diagnosed with prostate cancer and nearly 11,000 die in the UK each year.
During the trial, being run across Britain and Switzerland, 2,962 men took part in the trial and some were given six doses of docetaxol at the start of their treatment.
Overall, patients who received the drug lived 10 months longer, but for patients where the cancer had already spread beyond the pelvis, the increase in life expectancy was 22 months.
Prof Nicholas James, one of the researchers at Warwick University, called for all patients with prostate cancer that had spread to be given Docetaxel when they are diagnosed.
He said the NHS needed to act quickly: "To see a 22-month survival advantage off six lots of treatment given several years earlier is a very big benefit. We are very pleased by it."
Fellow researcher Prof Malcolm Mason, from Cardiff University, added: "In prostate cancer it has been used at a much more advanced stage of the illness, for some years, now we know that this chemotherapy should be added earlier, in fact as soon as hormone therapy starts."
It would be relatively cheap to do as Docetaxol is out of patent.
Experts said the findings from a trial in Britain and Switzerland were "potentially game-changing".
More than 40,000 men are diagnosed with prostate cancer and nearly 11,000 die in the UK each year.
During the trial, being run across Britain and Switzerland, 2,962 men took part in the trial and some were given six doses of docetaxol at the start of their treatment.
Overall, patients who received the drug lived 10 months longer, but for patients where the cancer had already spread beyond the pelvis, the increase in life expectancy was 22 months.
Prof Nicholas James, one of the researchers at Warwick University, called for all patients with prostate cancer that had spread to be given Docetaxel when they are diagnosed.
He said the NHS needed to act quickly: "To see a 22-month survival advantage off six lots of treatment given several years earlier is a very big benefit. We are very pleased by it."
Fellow researcher Prof Malcolm Mason, from Cardiff University, added: "In prostate cancer it has been used at a much more advanced stage of the illness, for some years, now we know that this chemotherapy should be added earlier, in fact as soon as hormone therapy starts."
It would be relatively cheap to do as Docetaxol is out of patent.
Wednesday, May 13, 2015
Canadian scientists discover new molecules that Kill Cancer
A new family of molecules that kill cancer cells and protect healthy
cells could be used to treat a number of different cancers, including
cervical, breast, ovarian and lung cancers.The researchers studied the process of DNA damage using a sort of
molecular filming technique called femto-second time-resolved laser
spectroscopy. The technique is like a high-speed camera, which uses two
pulses of light: one to start a reaction, and the other to monitor the
way the molecules react. This technique let researchers watch how
molecules interact in real-time, revealing how cells become cancerous.
This potential new field is being dubbed femtomedicine (FMD).
"We know DNA damage is the initial and crucial step in the development of cancer," said Professor Qing-Bin Lu, lead author of the study from the University of Waterloo, Canada. "With the FMD approach we can go back to the very beginning to find out what causes DNA damage in the first place, then mutation, then cancer. FMD is promising as an efficient, economical and rational approach for discovering new drugs, as it can save resources required to synthesize and screen a large library of compounds."When the FMD compounds enter a cancer cell, they react strongly and form reactive radicals, which cause the cell to kill itself. When the FMD compounds enter a healthy cell, the cell starts to increase the amount of a protective molecule called glutathione (GSH) in the cell. This protects the cell against chemical toxins, so it is not damaged.
This potential new field is being dubbed femtomedicine (FMD).
"We know DNA damage is the initial and crucial step in the development of cancer," said Professor Qing-Bin Lu, lead author of the study from the University of Waterloo, Canada. "With the FMD approach we can go back to the very beginning to find out what causes DNA damage in the first place, then mutation, then cancer. FMD is promising as an efficient, economical and rational approach for discovering new drugs, as it can save resources required to synthesize and screen a large library of compounds."When the FMD compounds enter a cancer cell, they react strongly and form reactive radicals, which cause the cell to kill itself. When the FMD compounds enter a healthy cell, the cell starts to increase the amount of a protective molecule called glutathione (GSH) in the cell. This protects the cell against chemical toxins, so it is not damaged.
Hormone Therapy for Prostate Cancer may impair thinking
Men undergoing hormone therapy to treat Prostate Cancer may experience impaired mental function within the first six months that persists for at least a year, a new study suggests.
The risk of memory, learning and
concentration problems associated with hormone therapy was greatest for
men with a particular gene mutation, researchers from the University of
South Florida in Tampa found.
Hormone therapy is used to lower the level of testosterone, thus preventing growth of prostate cancer cells.
"There is something about the treatment that seems
to be associated with worse mental function," said lead researcher Brian
Gonzalez, a postdoctoral fellow at the Moffitt Cancer Center in Tampa.
Fuzzy mental functioning was worse for men receiving hormone-depletion
therapy. But men with the gene mutation rs1047776 were 14 times more
likely to have mental problems related to hormone therapy than men
without this mutation
Tuesday, May 12, 2015
Radiation and hormonal therapy improves survival Prostate Cancer
A new study finds that men with Prostate Cancer that has spread to
nearby lymph nodes, who have a significant risk of dying from the
disease, can benefit from the addition of radiation therapy to
treatments that block the effects of testosterone. The findings imply
that the almost half of patients with node-positive disease nationwide
who this study found had not received combination therapy were not
receiving the treatment that could best control their tumor and possibly
save their lives "Our analysis of a large national database revealed that adding
radiation therapy to androgen-deprivation therapy decreased the risk of
death in these patients by 50 percent over five years," says Jason
Efstathiou, MD, DPhil, of the MGH Cancer Center and Department of
Radiation Oncology, senior author of the study. "It appears that more
aggressive local management of prostate cancer confined to the pelvis
can offer more durable disease control, prevent the disease from
spreading further and, for some patients, even provide a potential
cure."
"Our analysis of a large national database revealed that adding radiation therapy
to androgen-deprivation therapy decreased the risk of death in these
patients by 50 percent over five years," says Jason Efstathiou, MD,
DPhil, of the MGH Cancer Center and Department of Radiation Oncology,
senior author of the study. "It appears that more aggressive local
management of prostate cancer confined to the pelvis can offer more
durable disease control, prevent the disease from spreading further and,
for some patients, even provide a potential cure."
"Our analysis of a large national database revealed that adding radiation therapy
to androgen-deprivation therapy decreased the risk of death in these
patients by 50 percent over five years," says Jason Efstathiou, MD,
DPhil, of the MGH Cancer Center and Department of Radiation Oncology,
senior author of the study. "It appears that more aggressive local
management of prostate cancer confined to the pelvis can offer more
durable disease control, prevent the disease from spreading further and,
for some patients, even provide a potential cure."
"Our analysis of a large national database revealed that adding radiation therapy
to androgen-deprivation therapy decreased the risk of death in these
patients by 50 percent over five years," says Jason Efstathiou, MD,
DPhil, of the MGH Cancer Center and Department of Radiation Oncology,
senior author of the study. "It appears that more aggressive local
management of prostate cancer confined to the pelvis can offer more
durable disease control, prevent the disease from spreading further and,
for some patients, even provide a potential cure."
Lilly joins with German biotech firm in Cancer-fighting deal
Eli Lilly and Company and BioNTech AG announced that they have signed a research
collaboration agreement for the discovery of novel cancer
immuno-therapies.Under this partnership, both companies will work on identifying and
validating novel tumor targets and their corresponding T cell
receptors (TCRs) in one or more types of cancer.
Eli Lilly will make a $30 million equity investment
in BioNTech's subsidiary, Cell & Gene Therapies GmbH, which
specializes in the research and development of TCR and chimeric
antigen receptor immunotherapeutics. Additionally, Eli Lilly will
pay development, regulatory and commercial milestones of over $300
million for each potential therapy developed under this
collaboration, apart from a signing fee of $30 million. Upon the
successful commercialization of the drugs, BioNTech will be
entitled to receive tiered royalty payments in up to double digits.
Monday, May 11, 2015
Cuba's $1 per shot Cancer Treatment name released
“Investigators from around the world are trying to crack the nut of
cancer,” Feinstein Institute for Medical Research biologist Thomas
Rothstein, who worked for six years with the Cuban Center for Molecular
Immunology on a different vaccine for the same type of cancer, said.
“The Cubans are thinking in ways that are novel and clever.”
In Cuba, lung cancer is the fourth-leading cause of death, the publication reveals, which explains why researchers in the region have been looking into finding better cures for the disease.
Other countries in Europe and Japan have started clinical trials for Cimavax, that is the name of the Cuban “cutting-edge” vaccine that’s been 25 years in the making, and which costs the Cuban government just $1 per shot. The drug has been available as a free of charge cancer treatment since 2011 when it was released to the public.
The vaccine is very exciting for many other countries partly because it’s cheap to mass produce and store. Furthermore, by studying Cimavax, researchers could come up with similar therapies for other types of cancer, something the Cuban institute has not done yet.
In Cuba, lung cancer is the fourth-leading cause of death, the publication reveals, which explains why researchers in the region have been looking into finding better cures for the disease.
Other countries in Europe and Japan have started clinical trials for Cimavax, that is the name of the Cuban “cutting-edge” vaccine that’s been 25 years in the making, and which costs the Cuban government just $1 per shot. The drug has been available as a free of charge cancer treatment since 2011 when it was released to the public.
The vaccine is very exciting for many other countries partly because it’s cheap to mass produce and store. Furthermore, by studying Cimavax, researchers could come up with similar therapies for other types of cancer, something the Cuban institute has not done yet.
UK team identifies new targets for Cancer Treatments
New cancer treatments could be developed following a breakthrough in
research carried out by scientists at the University of Leicester.The experts, who led an international consortium of scientists, have identified key steps in cell division. Understanding how the cells divide will enable the development of treatments.Two
papers published in the Journal of Cell Biology have arisen from
research led by Professor Andrew Fry at the University of Leicester. Prof Fry, who is director of research in the College of Medicine,
Biological Sciences and Psychology at Leicester, said: "Together, these
two papers provide exciting insights on how cells ensure that they pass
on the right amount of genetic material to their offspring when they
divide. "They also highlight potential new targets for the development of novel cancer treatments."These papers identify a series of key steps that orchestrate the
mechanics of cell division and highlight novel targets that could be
inhibited to block cancer cell division.The study on cell division is funded by Worldwide Cancer Research,
Cancer Research UK, the Wellcome Trust, the Biotechnology and Biological
Sciences Research Council, Medical Research Council and Hope Against
Cancer, the Leicestershire charity.
New type of blood test is transforming Cancer Treatment
A new type of blood test is starting to transform cancer
treatment, sparing some patients the surgical and needle biopsies long
needed to guide their care.
The tests, called liquid biopsies, capture cancer cells or
DNA that tumors shed into the blood, instead of taking tissue from the
tumor itself. A lot is still unknown about the value of these tests, but
many doctors think they are a big advance that could make personalized
medicine possible for far more people.
They give the first noninvasive way to repeatedly sample a
cancer so doctors can profile its genes, target drugs to mutations, tell
quickly whether treatment is working, and adjust it as the cancer
evolves. The tests are mostly used when a tissue biopsy can’t easily be done,
when the cancer’s original site isn’t known, or when drugs have stopped
working and doctors are unsure what to try next, said Dr. Scott Kopetz, a
colon cancer specialist at MD Anderson. The tests are catching on
“faster than I anticipated,” he said.
Friday, May 8, 2015
Existing drug may treat deadliest Childhood Brain Tumor
The drug restricted the tumor’s growth in a lab dish and improved the
survival time of mice that had the tumor implanted into their brains,
according to researchers at the Stanford University School of Medicine,
in collaboration with colleagues at other institutions. The work is
noteworthy because the disease, a brain stem cancer called Diffuse Intrinsic Pontine Glioma, is nearly always fatal and lacks an effective
treatment.
“There have been over 200 clinical trials of chemotherapy drugs for
DIPG, and none have shown any survival benefit,” said Michelle Monje,
MD, PhD, assistant professor of neurology at Stanford and a senior
author of the paper. “But those trials were conducted before we knew
anything about the unique biology of this tumor.”
While the preclinical data in the new study are encouraging, Monje
cautioned that the drug, Panobionstat, needs further testing in a
closely monitored human clinical trial. The research team is now
planning such a trial in children with DIPG. Panobinostat was recently
approved by the Food and Drug Administration for treatment of a form of
blood cancer.
The drug repairs a portion of the cellular machinery now known to
be defective in DIPG tumor cells, the new research showed. “A key thing
that is wrong with DIPG cancer cells gets corrected by panobinostat,”
said Monje.
DIPG affects 200-400 school-aged children in the United States each year
and has a five-year survival rate of less than 1 percent; half of
patients die within nine months of diagnosis.
Lung Cancer drug Zykadia gains EU approval
Novartis announced today that the European Commission has approved
Zykadia(R) (ceritinib) to treat adult patients with anaplastic lymphoma
kinase (ALK)-positive advanced non-small cell lung cancer (NSCLC)
previously treated with crizotinib[1]. The approval of Zykadia in the
European Union (EU) provides patients with advanced ALK+ NSCLC
previously treated with crizotinib a new treatment option that
specifically targets the genetic makeup of their cancer.
"Molecular testing for genetic drivers in lung cancer plays a critical role as patients and physicians determine how to proceed with therapies, especially after they have experienced disease progression following initial treatment," said Stefania Vallone, international relations, Women Against Lung Cancer in Europe and board member, Lung Cancer Europe (LuCE). "Patients with resistant ALK+ NSCLC have had very few treatment options available that specifically target the genetic makeup of their disease. The approval of Zykadia brings new hope to the lung cancer community as we continue to advocate for innovative therapies."
"Molecular testing for genetic drivers in lung cancer plays a critical role as patients and physicians determine how to proceed with therapies, especially after they have experienced disease progression following initial treatment," said Stefania Vallone, international relations, Women Against Lung Cancer in Europe and board member, Lung Cancer Europe (LuCE). "Patients with resistant ALK+ NSCLC have had very few treatment options available that specifically target the genetic makeup of their disease. The approval of Zykadia brings new hope to the lung cancer community as we continue to advocate for innovative therapies."
Cancer drugs approved quickly but not to patient's benefit
Highly priced cancer drugs get rushed approvals despite poor trial
methodology and little effect on the longevity of patients, cautions
York University Professor Dr. Joel Lexchin in the School of Health
Policy and Management.
"Patients and their doctors should demand that regulators require pharma companies to provide clear evidence of clinical effectiveness of the drugs, resulting from rigorous methodology," suggests Lexchin. "Drug agencies like the Food and Drug Administration (FDA) and the European Medicine Agency (EMA) don't actually look at whether people live longer."
Lexchin cites earlier research reviewing solid cancer drugs within 10 years of EMA approval to point out that these drugs improved survival by just over a month.
"Similarly 71 drugs approved by the FDA from 2002 to 2014 for solid tumors have resulted in median gains in progression-free and overall survival of only 2.5 and 2.1 months, respectively," he says adding, "Also, only 42 per cent met the American Society of Clinical Oncology Cancer Research Committee's criteria for meaningful results for patients."
The Big pharma companies are having an easy ride with the European and US regulators, who are allowing them to test cancer drugs using surrogate measures instead of survival and other patient-centered measures.
"Patients and their doctors should demand that regulators require pharma companies to provide clear evidence of clinical effectiveness of the drugs, resulting from rigorous methodology," suggests Lexchin. "Drug agencies like the Food and Drug Administration (FDA) and the European Medicine Agency (EMA) don't actually look at whether people live longer."
Lexchin cites earlier research reviewing solid cancer drugs within 10 years of EMA approval to point out that these drugs improved survival by just over a month.
"Similarly 71 drugs approved by the FDA from 2002 to 2014 for solid tumors have resulted in median gains in progression-free and overall survival of only 2.5 and 2.1 months, respectively," he says adding, "Also, only 42 per cent met the American Society of Clinical Oncology Cancer Research Committee's criteria for meaningful results for patients."
The Big pharma companies are having an easy ride with the European and US regulators, who are allowing them to test cancer drugs using surrogate measures instead of survival and other patient-centered measures.
Thursday, May 7, 2015
Statins stop Prostate Cancer from progressing
The researchers report that men who had been taking statins since the start of androgen deprivation therapy
(ADT) went a median of 27.5 months before their disease began to
worsen, compared to 17.4 months for men who didn't take statins. The
trial involved 926 patients, 70 percent of whom had their disease
progress during a six-year period.
"This median 10-month benefit in delaying disease progression suggests that statins could be a valuable addition to our current therapies for prostate cancer," says the study's first author, Lauren Harshman, MD, medical oncologist at the Lank Center for Genitourinary Oncology at Dana-Farber. "These results are supported by multiple prior epidemiologic studies demonstrating that statin use may be associated with improved outcomes in prostate cancer, but require validation."
The trial grew out of laboratory studies that suggested statins could delay prostate cancer growth in patients receiving ADT. (ADT reduces the amount of androgen in the body, preventing prostate cancer cells from using it to fuel their growth. For many years, it has been the frontline treatment for patients with hormone-sensitive prostate cancer that has spread beyond the prostate gland.)
"This median 10-month benefit in delaying disease progression suggests that statins could be a valuable addition to our current therapies for prostate cancer," says the study's first author, Lauren Harshman, MD, medical oncologist at the Lank Center for Genitourinary Oncology at Dana-Farber. "These results are supported by multiple prior epidemiologic studies demonstrating that statin use may be associated with improved outcomes in prostate cancer, but require validation."
The trial grew out of laboratory studies that suggested statins could delay prostate cancer growth in patients receiving ADT. (ADT reduces the amount of androgen in the body, preventing prostate cancer cells from using it to fuel their growth. For many years, it has been the frontline treatment for patients with hormone-sensitive prostate cancer that has spread beyond the prostate gland.)
UK Cancer researchers create 1st Living Bio-bank
Scientists have created the world’s first “living biobank”
of patients’ tumors and used the tissue to identify the most promising
drugs for each person’s disease. Tiny biopsies of the patients’ tumors were grown into
clumps of cells and kept alive in the lab, so researchers could study
their specific mutations and subject the tumors to more than 80
anti-cancer drugs.
Geneticists at the Wellcome Trust Sanger Institute in Cambridge said the work marked a step towards more personalized medical treatments that target cancer tumor by tumor in individual patients.The researchers grew what they call 3D organoids from both cancerous and healthy tissue biopsies taken from 20 patients with bowel cancer. All of the patients had received surgery to remove their tumors and were not having further treatment.
“The beautiful thing here is that we’ve shown we can grow these organoids in the lab and they look a lot like the tissue from which they were taken, so they should be much better models for studying cancer,” said Mathew Garnett, a researcher at the Sanger Institute.
“This opens up amazing opportunities to ask questions about the biology of the patients’ tumors, the genetics of their tumors, and to see how that patient might respond to different cancer drugs,” he added. About 41,000 people in the UK are diagnosed with bowel cancer each year.
Geneticists at the Wellcome Trust Sanger Institute in Cambridge said the work marked a step towards more personalized medical treatments that target cancer tumor by tumor in individual patients.The researchers grew what they call 3D organoids from both cancerous and healthy tissue biopsies taken from 20 patients with bowel cancer. All of the patients had received surgery to remove their tumors and were not having further treatment.
“The beautiful thing here is that we’ve shown we can grow these organoids in the lab and they look a lot like the tissue from which they were taken, so they should be much better models for studying cancer,” said Mathew Garnett, a researcher at the Sanger Institute.
“This opens up amazing opportunities to ask questions about the biology of the patients’ tumors, the genetics of their tumors, and to see how that patient might respond to different cancer drugs,” he added. About 41,000 people in the UK are diagnosed with bowel cancer each year.
CAR T cell Cancer therapies
New therapies that clinical data show can eliminate blood cancers such as Leukemia and Lymphoma in 40 percent to 90 percent of patients may have to be genetically modified to include a switch that shields healthy cells from attack. The therapies involve using what are known as CAR T cells, which are white blood cells taken from the body and genetically modified to have the cancer-spotting traits of antibodies. These cells can circulate inside a person for years, even a lifetime, relentlessly seeking out cancerous growth.
Although, a third of the patients in some trials given CAR T cells have developed life-threatening fevers and inflammation. Doctors say the reason is that the modified T cells cause inflammation because they kill so many cancer cells so quickly. Another concern is that when the therapies are eventually targeted at solid tumors such as lung or kidney cancer, they could also attack healthy cells containing the same protein that's the target of the anti-cancer therapy.
Drugmakers are building in "switches" to suppress CAR T cells if serious side effects emerge, or to make them self-destruct if they attack healthy tissue. The switches involve an additional receptor on the CAR T cell that can be controlled by giving the patient a second medication, such as the widely-used cancer drug Rituxan. The so-called suicide switches being developed for CAR T cells are a refinement of the body's own natural process of apoptosis, by which defective or unneeded cells are programmed to self-destruct. Approval of the new therapies to combat blood cancers are not expected for another three or four years, analysts said. Approval for therapies to fight solid tumors will take years longer, they said.
Wednesday, May 6, 2015
Venetoclax receives Breakthrough Therapy Designation
AbbVie today announced its investigational medicine Venetoclax, an inhibitor
of the B-cell lymphoma-2 (BCL-2) protein that is being developed in
partnership with Genentech and Roche, has been granted Breakthrough Therapy Designation by the FDA
for the treatment of chronic lymphocytic leukemia (CLL) in previously
treated (relapsed/refractory) patients with the 17p deletion genetic
mutation.
CLL is a slow-progressing cancer of the bone marrow and blood in which the bone marrow makes too many lymphocytes, a type of white blood cell. CLL accounts for approximately one quarter of the new cases of Leukemia diagnosed in the United States. Approximately 3-10 percent of CLL patients have 17p deletion at diagnosis, and it occurs in 30-50 percent of patients with relapsed/refractory CLL. The 17p deletion mutation is a genomic alteration in which a part of chromosome 17 is absent.4 The median life expectancy for CLL patients with 17p deletion is less than 2-3 years.
Venetoclax is an investigational oral B-cell Lymphoma-2 (BCL-2) inhibitor being evaluated for the treatment of patients with various cancer types. The BCL-2 protein prevents apoptosis of some cells, including lymphocytes, and can be expressed in some cancer types. Venetoclax is designed to selectively inhibit the function of the BCL-2 protein. Venetoclax is being developed in collaboration with Genentech and Roche.
CLL is a slow-progressing cancer of the bone marrow and blood in which the bone marrow makes too many lymphocytes, a type of white blood cell. CLL accounts for approximately one quarter of the new cases of Leukemia diagnosed in the United States. Approximately 3-10 percent of CLL patients have 17p deletion at diagnosis, and it occurs in 30-50 percent of patients with relapsed/refractory CLL. The 17p deletion mutation is a genomic alteration in which a part of chromosome 17 is absent.4 The median life expectancy for CLL patients with 17p deletion is less than 2-3 years.
Venetoclax is an investigational oral B-cell Lymphoma-2 (BCL-2) inhibitor being evaluated for the treatment of patients with various cancer types. The BCL-2 protein prevents apoptosis of some cells, including lymphocytes, and can be expressed in some cancer types. Venetoclax is designed to selectively inhibit the function of the BCL-2 protein. Venetoclax is being developed in collaboration with Genentech and Roche.
Trial of new Skin Cancer Drug begins
The trial is the culmination of a pioneering research programme to
design, synthesise and develop the new drug class, led by scientists at
The Institute of Cancer Research, London, and the Cancer Research UK
Manchester Institute at The University of Manchester.
It is starting just three months after a major publication in the journal Cancer Cell described the potential of this new drug class, which is potentially able to treat Melanomas, the most serious type of skin cancer, that do not respond or have become resistant to existing therapies.
The
phase I trial of the drug, which is yet to be given a formal name and
is currently known as BAL3833/CCT3833, is sponsored by The Institute of
Cancer Research (ICR) and The Royal Marsden NHS Foundation Trust. The
trial is funded by the Wellcome Trust, the NIHR Biomedical Research
Centre at The Royal Marsden and the ICR, The Christie charity and the
Cancer Research UK Manchester Institute. The first
patient began treatment at The Royal Marsden, with patients also to be
treated at The Christie NHS Foundation Trust in Manchester.
Just
last month, a new consortium was announced to develop this drug class
for patients, following an agreement between academic organisations,
funders and Swiss-based biopharmaceutical company Basilea Pharmaceutica
International Ltd.
The trial will recruit around 25 patients with advanced, solid tumors, focusing on advanced Melanoma, with the aim of establishing the safe maximum dose for a planned phase II clinical trial.
Prostate Cancer could be 'wiped out' by new treatment
A new therapy that boosts the immune system could wipe advanced prostate cancer, early research suggests. In mice, human disease tumors were "almost completely destroyed" by the animals' own immune systems, scientists said.
The treatment, dubbed "chemoimmunotherapy", involved low doses of the
drug Oxaliplatin which has a unique ability to activate cancer-killing
immune cells. Equally important to the treatment was removing or
blocking immune system cells that put a brake on the body's defences.
Each year in the UK around 41,000 men are diagnosed with prostate cancer and 11,000 die from the disease. The immunosuppressive "B-cells" are especially abundant in the tumors of men who have advanced and spreading prostate cancer.
Such cells can render conventional therapies ineffective and allowing tumors to grow unchecked. Because of immunosuppression, advanced and aggressive prostate cancer does not typically respond to chemotherapy. US lead scientist Dr Shabnam Shalapour, from the University of California at San Diego, said the new approach should now be tested clinically.
"This indicates that B-cell-mediated immunosuppression might be the reason several other cancers are also unresponsive to checkpoint inhibitors, raising the hope that chemoimmunotherapy will have broader applications for many cancer types."
Canadian research found prostate cancer sufferers treated with tiny radioactive implants are twice as likely to be cancer-free as those given conventional therapy after five years.
Tuesday, May 5, 2015
New drugs against Advanced Lung Cancer
Researchers tested the drug
AZD9291. They found that among 127 patients with a T790M mutation, the
response rate was 61 percent. Most patients went at least six months
with No Cancer Progression,
and half went about 10 months or longer. That second figure is similar
to what's seen with Tarceva (erlotinib), one of the first-line epidermal
growth factor receptor (EGFR) inhibitors, Pasi Janne, M.D., Ph.D., lead
researcher on the study, stated. Janne is an oncologist at the Dana-Farber Cancer Institute in Boston.
"So if you give this after a patient becomes resistant (to an EGFR inhibitor), you're doubling the time that they're on a drug that works," Janne said. Just as important, he said, the new drug is better tolerated than EGFR medication, without the potentially severe skin effects of those drugs. Six percent of patients did have a "serious adverse event" thought to be caused by the medication. But the most common side effects were diarrhea, nausea, and rash, which were manageable, Janne said.
The second study, of an oral drug called Rociletinib, had similar results. Among patients with a T790M mutation, the response rate was 59 percent. Hyperglycemia, diarrhea, nausea, and rash were the most common side effects.
AstraZeneca, the developer of AZD9291, funded the first study, and Janne has served as a consultant to the company.
"So if you give this after a patient becomes resistant (to an EGFR inhibitor), you're doubling the time that they're on a drug that works," Janne said. Just as important, he said, the new drug is better tolerated than EGFR medication, without the potentially severe skin effects of those drugs. Six percent of patients did have a "serious adverse event" thought to be caused by the medication. But the most common side effects were diarrhea, nausea, and rash, which were manageable, Janne said.
The second study, of an oral drug called Rociletinib, had similar results. Among patients with a T790M mutation, the response rate was 59 percent. Hyperglycemia, diarrhea, nausea, and rash were the most common side effects.
AstraZeneca, the developer of AZD9291, funded the first study, and Janne has served as a consultant to the company.
Exercise helps in Cancer treatment
A Kansas State University researcher has found that fast-walking or a
light jogging on a regular basis can improve cancer treatments.
Behnke and his co-researchers had a $750,000 American Cancer Society grant and found that moderate exercise improves blood flow to tumors and enhances the effectiveness of radiation treatments. Existing research has found that moderate exercise can also help cancer patients counteract some negative side effects of treatment like fatigue, low blood count and muscle atrophy.
But Behnke said that too much exercise can be counter-productive.
Behnke and his co-researchers had a $750,000 American Cancer Society grant and found that moderate exercise improves blood flow to tumors and enhances the effectiveness of radiation treatments. Existing research has found that moderate exercise can also help cancer patients counteract some negative side effects of treatment like fatigue, low blood count and muscle atrophy.
But Behnke said that too much exercise can be counter-productive.
IBM’s Watson will be taking on Cancer next with Targeted Therapies
IBM’s trivia-smart, cloud-based Watson computer system is taking on its next
opponent: cancer.
Fourteen U.S. and Canadian cancer institutes are set to utilize the super machine’s knowledge to select targeted therapies based on a tumor’s genes, IBM announced today.
The technology will allow clinicians to upload a patient’s DNA to Watson, which will then identify which genes are mutated or responsible for the Cancer.
“The solution is going to be Watson or something like it,” oncologist Norman Sharpless of the University of North Carolina Lineberger Cancer Center told Reuters. “Humans alone can't do it.”
The initial phase of the program will include several types of mutations, including those found in lymphoma, melanoma, pancreatic, ovarian, brain, lung, breast and colorectal cancer.
IBM announced that Ann & Robert H. Lurie Children’s Hospital of Chicago; BC Cancer Agency; City of Hope; Cleveland Clinic; Duke Cancer Institute; Fred & Pamela Buffett Cancer Center in Omaha, Nebraska; McDonnell Genome Institute at Washington University in St. Louis; New York Genome Center; Sanford Health; University of Kansas Cancer Center; University of North Carolina Lineberger Cancer Center; University of Southern California Center for Applied Molecular Medicine; University of Washington Medical Center; and Yale Cancer Center will begin using Watson for this project by late 2015
Fourteen U.S. and Canadian cancer institutes are set to utilize the super machine’s knowledge to select targeted therapies based on a tumor’s genes, IBM announced today.
The technology will allow clinicians to upload a patient’s DNA to Watson, which will then identify which genes are mutated or responsible for the Cancer.
“The solution is going to be Watson or something like it,” oncologist Norman Sharpless of the University of North Carolina Lineberger Cancer Center told Reuters. “Humans alone can't do it.”
The initial phase of the program will include several types of mutations, including those found in lymphoma, melanoma, pancreatic, ovarian, brain, lung, breast and colorectal cancer.
IBM announced that Ann & Robert H. Lurie Children’s Hospital of Chicago; BC Cancer Agency; City of Hope; Cleveland Clinic; Duke Cancer Institute; Fred & Pamela Buffett Cancer Center in Omaha, Nebraska; McDonnell Genome Institute at Washington University in St. Louis; New York Genome Center; Sanford Health; University of Kansas Cancer Center; University of North Carolina Lineberger Cancer Center; University of Southern California Center for Applied Molecular Medicine; University of Washington Medical Center; and Yale Cancer Center will begin using Watson for this project by late 2015
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